Impact Factor
3.79
Journal Citation Impact
Estimated influence, citation density, publishing volume, and citation integrity from the analytics table.
Citation rate
4.31
1,441 total citations
h5-index
42
h5 depth signal
Cited share
69.2%
243 of 351
Total citations
1,441
Citation footprint
Metric signal
4.04
External metric anchor
Self-citation
6.3%
91 self-citations
Citations Trend
Monthly Publications Cadence
Citing Geographic Demographics
Germany
431
United States
319
Denmark
207
China
178
Sweden
124
Citing Fields of Research
Physiology
519
Cardiology
198
Cell Biology
196
Kidney Diseases
174
Diabetes
160
Publishing Activity & Reach
Volume, recency, access pattern, and citing-community signals from the journal analytics record.
All-time article footprint
3,566
Articles tracked across the journal lifetime
Indexed publication set
351
243 cited publications
Last 12 months
209
17.4 publications/month
Open access share
51.2%
107 OA publications in the last year
Leading citing country
Germany
431 citing publications
Leading citing field
Physiology
519 citing publications
Latest tracked publication
12 October 2026
10 recent records available
Coverage & Indexing History
v186n1, Jan. 2006-
v186n1, Jan. 2006-
Research Focus & Classification
Indexed Subjects
Physiology
Diabetes
Kidney Diseases
Cardiology
Neurosciences
Musculoskeletal Disorders
Issuing & Sponsoring Bodies
Contributor
Scandinavian Society for Physiology
Contributor
Federation of European Physiological Societies
Broad Categories
Physiology
Musculoskeletal Disorders
Urology
Diabetes
Mitochondria
Cardiology
Inflammatory Bowel Diseases & Infections
MeSH Descriptors
Physiological Phenomena
Latest Publications
Recent article records with DOI-first linking and condensed abstracts.
01
DOI 10.1111/apha.70332
Open DOI
Sex Hormone‐Binding Globulin Limits Glucocorticoid‐Induced Muscle Wasting by Preserving Estrogen‐Dependent Repression of Catabolic Signaling
Aim: Chronic glucocorticoid (GC) therapy induces severe metabolic complications, notably secondary sarcopenia driven by excessive glucocorticoid receptor (GR)‐mediated catabolism. Although sex steroids protect skeletal muscle metabolism,...
02
DOI 10.1111/apha.70330
Open DOI
ITCHing To Halt Muscle Atrophy
03
DOI 10.1111/apha.70308
Open DOI
Renal Myeloid Mechanisms, Cross‐Talk in Hypertension
Hypertension involves an impairment of renal sodium excretion along with activation of pro‐inflammatory responses in the kidney. Dendritic cells (DCs) are professional antigen‐presenting cells that sense disturbances in cell and tissue h...
04
DOI 10.1111/apha.70318
Open DOI
Maresin 2 Attenuates Hypertensive Vascular Remodeling via Inhibiting Macrophage Infiltration and Pro‐fibrotic Polarization
Immune‐inflammatory responses are pivotal regulators of hypertensive vascular remodeling. Specialized pro‐resolving mediators (SPMs), including Maresin 2 (MaR2), are endogenous anti‐inflammatory molecules. However, the specific role of M...
05
06
DOI 10.1111/apha.70329
Open DOI
Acute Kidney Injury and Chronic Kidney Disease
07
DOI 10.1111/apha.70325
Open DOI
Klotho Deficiency Impairs Distal Potassium Homeostasis Through mTORC1 ‐Dependent Suppression of ROMK
Aim: Hyperkalemia is prevalent in the elderly, and underlying molecular mechanisms remain incompletely understood. We hypothesized that Klotho deficiency, a feature of aging, impairs renal potassium homeostasis and contributes to hyperka...
08
09
DOI 10.1111/apha.70327
Open DOI
Fibroblast Growth Factor 2 Enhances Contraction of Arterioles in the Medulla Oblongata and the Basilar Artery in Mice With Chronic Kidney Disease
Aim: Chronic kidney disease (CKD) augments vascular contractility in multiple vascular beds. Fibroblast growth factor 2 (FGF2), whose expression is upregulated in CKD, acts pro‐contractile by supporting vasoconstrictor capacity. Thus, th...
10
DOI 10.1111/apha.70326
Open DOI
Does the Heart Pace to the Drumbeat of Phosphate?
Bibliographical & Catalog Notes
Title from cover.
Print issues ceased with 2013.
Also issued online.
Official journal of the Federation of European Physiological Societies (FEPS).
Published on behalf of the Scandinavian Physiological Society.